目的：探讨小胶质细胞吞噬α‐突触核蛋白的分子机制。方法构建α‐Syn寡聚体诱导BV‐2细胞活化模型，免疫荧光检测BV‐2细胞内α‐Syn阳性包涵体的数量。Western blot检测BV‐2细胞LRRK2蛋白的表达。Pull down检测BV‐2细胞Rac1、Cdc42、RhoA的活性。结果与对照组相比，α‐Syn寡聚体诱导BV‐2细胞内α‐Syn阳性包涵体数量增加，LRRK2蛋白表达增加及Rac1、Cdc42、RhoA活性增加。结论小胶质细胞对α‐突触核蛋白的吞噬与LRRK2活化Rho GTPases信号通路相关。%Objective To investigate the mechanism of microglial phagocytosis of α‐synuclein.Methods BV‐2 cells activa‐tion model induced by α‐synuclein oligomers was established. Immunofluorescence stain was performed to detect α‐synuclein‐positive inclusions in BV‐2 cells. Western blot was performed to detect LRRK2 expression in BV‐2 cells. Pull down was per‐formed to detect Rho GTPases signaling pathway activation in BV‐2 cells.Results Compared with the control group ,α‐synucle‐in‐positive inclusions ,LRRK2 expression and Rho GTPases signaling pathway activity in BV‐2 cells significantly increased in theα‐synuclein group.Conclusion The Rho GTPases signaling pathway activation induced by LRRK2 associate closely with mi‐croglial phagocytosis of α‐synuclein.
展开▼
